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Articles by S. G Ren
Total Records ( 2 ) for S. G Ren
  V Chesnokova , C Wong , S Zonis , A Gruszka , K Wawrowsky , S. G Ren , A BenShlomo and R. Yu

Pituitary tumor transforming gene (PTTG) encodes a securin protein critical in regulating chromosome separation. PTTG-null (PTTG–/–) mice exhibit pancreatic β-cell hypoplasia and insulinopenic diabetes. We tested whether PTTG deletion causes β-cell senescence, resulting in diminished β-cell mass. We examined β-cell mass, proliferation, apoptosis, neogenesis, cell size, and senescence in PTTG–/– and WT mice from embryo to young adulthood before diabetes is evident. The roles of cyclin-dependent kinase inhibitors and DNA damage in the pathogenesis of diabetes in PTTG–/– mice were also addressed. Relative β-cell mass in PTTG–/– mice began to decrease at 2–3 wk, whereas β-cell proliferation rate was initially normal but decreased in PTTG–/– mice beginning at 2 months. Apoptosis was also much more evident in PTTG–/– mice. At 1 month, β-cell neogenesis was robust in wild-type mice but was absent in PTTG–/– mice. In addition, the size of β-cells became larger and macronuclei were prominent in PTTG–/– animals. Senescence-associated β-galactosidase was also active in PTTG–/– β-cells at 1 month. Cyclin-dependent kinase inhibitor p21 was progressively up-regulated in PTTG–/– islets, and p21 deletion partially rescued PTTG–/– mice from development of diabetes. mRNA array showed that DNA damage-associated genes were activated in PTTG–/– islets. We conclude that β-cell apoptosis and senescence contribute to the diminished β-cell mass in PTTG–/– mice, likely secondary to DNA damage. Our results also suggest that ductal progenitor β-cells are exhausted by excessive neogenesis induced by apoptosis in PTTG–/– mice.

  G Vlotides , Y. H Chen , T Eigler , S. G Ren and S. Melmed

To investigate paracrine regulation of pituitary cell growth, we tested fibroblast growth factor (FGF) regulation of TtT/GF folliculostellate (FS) cells. FGF-2, and FGF-4 markedly induced cell proliferation, evidenced by induction of pituitary tumor transforming gene-1 (Pttg1) mRNA expression and percentage of cells in S phase. Signaling for FGF-2-induced FS cell proliferation was explored by specific pharmacological inhibition. A potent inhibitory effect on FGF-2 action was observed by blocking of Src tyrosine kinase with 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine (≥0.1 µm), followed by protein kinase C (PKC) inhibition with GF109203X. Treatment with FGF-2 (30 ng/ml; 10 min) activated phosphorylation of signal transducer and activator of transcription-3, ERK, stress-activated protein kinase/c-Jun N-terminal kinase, Akt, and focal adhesion kinase. Src inhibition with 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine suppressed FGF-2-induced Akt and focal adhesion kinase, indicating effects downstream of FGF-2-induced Src activation. FGF-2 also markedly induced its own mRNA expression, peaking at 2–4 h, and this effect was suppressed by Src tyrosine kinase inhibition. The PKC inhibitor GF109203X abolished FGF-2 autoinduction, indicating PKC as the primary pathway involved in FGF-2 autoregulation in these cells. In addition to pituitary FGF-2 paracrine activity on hormonally active cells, these results show an autofeedback mechanism for FGF-2 in non-hormone-secreting pituitary FS cells, inducing cell growth and its own gene expression, and mediated by Src/PKC signaling.

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